Toxicity Profiles

Condensed Toxicity Summary for MOLYBDENUM

NOTE: Although the toxicity values presented in these toxicity profiles were correct at the time they were produced, these values are subject to change. Users should always refer to the Toxicity Value Database for the current toxicity values.

*Managed by Martin Marietta Energy Systems, Inc., for the U.S. Department of Energy under
Contract No. DE-AC05-84OR21400.

Molybdenum (Mo) occurs naturally in various ores; the principal source being
molybdenite (MoS2) (Stokinger, 1981). Molybdenum compounds are used primarily in the
production of metal alloys. Molybdenum is considered an essential trace element; the
provisional recommended dietary intake is 75-250 g/day for adults and older children (NRC,
1989).

Water-soluble molybdenum compounds are readily taken up through the lungs and
gastrointestinal tract; but insoluble compounds are not. Following absorption, molybdenum is
distributed throughout the body with the highest levels generally found in the liver, kidneys,
spleen, and bone (Wennig and Kirsch, 1988). Limited data suggest that 25 to 50% of an oral
dose is excreted in the urine, with small amounts also eliminated in the bile. Biological half-life
may vary from several hours in laboratory animals to as much as several weeks in humans
(Friberg and Lener, 1986; Jarrell et al., 1980; Stokinger, 1981; Vanoeteren et al., 1982;
Venugopal and Luckey, 1978).

Data documenting molybdenum toxicity in humans are limited. The physical and
chemical state of the molybdenum, route of exposure, and compounding factors such as dietary
copper and sulfur levels may all affect toxicity. Mild cases of molybdenosis may be clinically
identifiable only by biochemical changes (eg., increases in uric acid levels due to the role of
molybdenum in the enzyme xanthine oxidase). Excessive intake of molybdenum causes a
physiological copper deficiency, and conversely, in cases of inadequate dietary intake of copper,
molybdenum toxicity may occur at lower exposure levels.

There is no information available on the acute or subchronic oral toxicity of
molybdenum in humans. In studies conducted in a region of Armenia where levels of
molybdenum in the soil are high (77 mg Mo/kg), 18% of the adults examined in one town and
31% of those in another town were found to have elevated concentrations of uric acid in the
blood and urine, increased blood xanthine oxidase activity, and gout-like symptoms such as
arthralgia, articular deformities, erythema, and edema (Kovalskii et al., 1961). The daily
molybdenum intake was estimated to be 10-15 mg. An outbreak of genu valgum (knock-knees)
in India was attributed to an increase in Mo levels in sorgum, the main staple food of the region.
The estimated daily Mo intake was 1.5 mg (Jarrell et al., 1980).

In animals, acutely toxic oral doses of molybdenum result in severe gastrointestinal
irritation with diarrhea, coma and death from cardiac failure. Oral LD50 values of 125 and 370
mg Mo/kg for molybdenum trioxide and ammonium molybdate, respectively, have been reported
in laboratory rats (Venugopal and Luckey, 1978). Subchronic and chronic oral exposures can
result in gastrointestinal disturbances, growth retardation, anemia, hypothyroidism, bone and
joint deformities, sterility, liver and kidney abnormalities, and death (Lloyd et al., 1976;
Venugopal and Luckey, 1978; Valli et al., 1969; Fairhall et al., 1945; Rana and Kumar, 1980).
Fatty degeneration of the liver occurred in rabbits dosed with 50 mg/kg/day for 6 mo
(Asmangulyan, 1965) and in rats dosed with 5 mg/kg/day as ammonium molybdate for 1 year
(Valjcuk and Sramko, 1973). Male sterility, was reported in rats fed diets containing 80 or 140
ppm Mo (Jeter and Davis, 1954). Teratogenic effects have not been observed in mammals, but
embryotoxic effects, including reduced weight gain, reduced skeletal ossification, nerve system
demyelinization, and reduced survival of offspring have been reported (Wide, 1984; Earl and
Vish, 1979; Schroeder and Mitchener, 1971).

The chronic oral Reference Dose (RfD) for molybdenum and molybdenum compounds
is 0.005 mg/kg/day, based on biochemical indices in humans (U.S. EPA, 1992). The subchronic
RfD is also 0.005 mg/kg/day (U.S. EPA, 1992).

Information on the inhalation toxicity of molybdenum in humans following acute and
subchronic exposures is not available. Studies of workers chronically exposed to Mo indicate a
high incidence of weakness, fatigue, headache, irritability, lack of appetite, epigastric pain, joint
and muscle pain, weight loss, red and moist skin, tremor of the hands, sweating, and dizziness
(Akopajan, 1964; Ecolajan, 1965; Walravens et al., 1979). Elevated levels of Mo in blood
plasma and urine and high levels of ceruloplasmin and uric acid in blood serum were reported
for workers exposed to Mo (8-hr TWA 9.5 mg Mo/m3) (Walravens et al., 1979). Occupational
exposure to molybdenum may also result in increased serum bilirubin levels and decreased blood
IgA/IgG ratios due to a rise in alpha-immunoglobulins (Avakajan, 1966b; 1968). Direct
pulmonary effects of chronic exposure to Mo have been reported in only one study in which 3 of
19 workers exposed to Mo and MoO3 (1 to 19 mg/m3) for 3-7 years were symptomatic and had
X-ray findings indicative of pneumoconiosis (Mogilevskaya, 1963). Adverse reproductive or
developmental effects have not been observed in molybdenum workers (Metreveli et al., 1985).

Subchronic and chronic Reference Concentrations (RfC) for molybdenum are not
available.

Information on the oral or inhalation carcinogenicity of molybdenum compounds in
humans was not available, and animal data indicate that Mo may have an inhibitory effect on
esophageal (Luo et al., 1983; van Rensburg et al., 1986; Komada, et al., 1990) and mammary
carcinogenesis (Wei et al., 1987). However, intraperitoneal injections of MoO3 in mice produced
a significant increase in the number of lung adenomas per mouse and an insignificant increase in
the number of mice bearing tumors (Stoner et al., 1976). Molybdenum is placed in EPA Group
D, not classifiable as to carcinogenicity in humans (U.S. EPA, 1990) and calculation of slope
factors is not possible.